Key result
Non-constant ventricular pacing can trigger polymorphic VT by altering activation sequences in pacemaker patients.
Case Report (n=1)
Demonstrates that proarrhythmia in pacemaker patients can occur independently of bradycardia due to altered ventricular activation sequences.
Alerts clinicians to pacing proarrhythmia beyond bradycardia; hypothesis-generating for activation-sequence mechanisms in permanent pacemakers.
Polymorphic ventricular tachycardia (torsades de pointes) can be associated with syncope or sudden cardiac death in patients with permanent pacemakers and ventricular pacing. These events are usually due to pacemaker malfunction or specific programming (e.g. MVP algorithm) leading to pauses and/or short-long-short sequences, which can cause marked QT prolongation and early afterdepolarisations (EADs). On some occasions, however, the proarrhythmia is not bradycardia dependent and is rather due to alterations in the ventricular activation sequence when the ventricular pacing is not constant, leading to changes in the ventricular depolarisation and in the absence of pauses or bradycardia.
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Lypourlis et al. (2025) conducted a case report in Polymorphic ventricular tachycardia (torsades de pointes) (n=1). Permanent pacemaker was evaluated. Alterations in the ventricular activation sequence due to non-constant ventricular pacing can cause non-bradycardia-dependent polymorphic ventricular tachycardia in patients with permanent pacemakers.
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